HLA class II association with Type I allergy to house dust mite and Japanese cedar pollen in Japanese subjects

ABSTRACTWe evaluated the incidence of the association of HLA class II phenotype and specific IgE responsiveness against house dust mite (HDM) and/or Japanese cedar pollen (Jc) in 176 patients with allergic rhinitis, with or without bronchial asthma, and 107 nonallergic subjects. Specific IgE antibody titration against the purified allergens Der f1 and Der f2 from HDM, and against Cry J1 and Cry J2 from Jc, was performed by using enzyme-linked immunosorbent assay (ELISA) and radioimmunoassay (RIA) in sera from all subjects. HLA class II oligotyping was performed by the polymerase chain reaction sequence specific oligonucleotide (PCR-SSO) method on the DRB1*, DQA1*, DQB1* and DPB1* alleles using peripheral blood cells. The high IgE responders ≥ class 4 to the purified allergens were identified by using the IgE antibody reference concentration obtained by ELISA, RIA and routine IgE CAP RAST. Compared to the controls, the patients with both rhinitis and asthma showed significantly higher frequencies of DRB1* 0901, DQB1* 0303, and DPB1* 0401 alleles. High IgE responsiveness to HDM was associated with DRB1* 1101, 0901, DQB1* 0303, and DPB1*0401 alleles. The patients with anti-Der f1 IgE antibody concentration exceeding 72.2 ng/mL showed significantly elevated frequencies for DQB1*0401 and DPB1*0401 alleles, and those with anti Der f2 IgE antibody concentration exceeding 46.2 ng/mL showed significantly elevated frequencies for DPB1*0401 and 0901 alleles. High IgE responsiveness to Jc with Cry j1 and Cryj2was associated with the DRB1* 1201 alleles

Anti-Dermatophagoides farinae type I and II IgE antibodies in allergic rhinitis

ABSTRACTSera from 27 patients with mite-sensitive allergic rhinitis, without atopic dermatitis and bronchial asthma, were examined for anti-Der f I and anti-Der f II IgE antibody contents by enzyme-linked immunosorbent assay (ELISA). Anti-Der f I and anti-Der f II IgE antibody levels were 14.78 ± 1.34 and 32.68 ± 0.88 ng/mL (mean ± SEM), respectively. The anti-Der f II IgE antibody was predominant over the anti-Der f I IgE antibody in these patients.In comparison with the results of a previous study the present study indicates that the ratio between serum anti-Der f I and II IgE antibodies in patients with allergic rhinitis indicated the same pattern as in that of patients with bronchial asthma, while the inverse was the case in patients with atopic dermatitis.These results indicate that immunological features and major allergen molecules could be different in different atopic diseases. At present it is not clear where this difference comes from, but the route of immunological sensitization (via respiratory tract vs via skin) might result in the difference

A novel hypothesis for the gene expression for the control of atopic and other hereditary diseases

The requirement of RNA polymerase proteins and transcription factor proteins for the expression of genetic information in DNA clearly indicates that the process is influenced by certain proteins in the body and/or in the environment, which is totally opposite to the 'central dogma' of Crick. In this article, we present a working hypothesis (helical hypothesis) that may explain the programmed nature of various biological events simply and naturally. Future investigations on the factors that regulate the gene transcription of cytokine clusters, including intereukin (IL)-4 and IL-5, may provide an answer for controlling atopic as well as other hereditary (genetic) diseases

Epstein-Barr Virus Infection in Childhood May Precipitate Atopic Diseases

Background: Epstein Barr virus (EBV) has been suspected of being involved in the development of atopy. There are several studies suggesting a positive as well as negative association between EBV infection and atopic diseases. Here, we carried out a large-scale, systematic investigation to address the issue of the possible association between EBV infection and atopic diseases. Methods: Anti-EBV-viral capsid antigen (VCA) antibody titer, anti-EBV nuclear antigen (EBNA) antibody titer, atypical lymphocyte (AtLy) count and EBV-DNA copy number in 106 WBC were examined as evidence for EBV infection, and characteristic parameters of atopic disease such as total serum immunoglobulin E (IgE) level, highest antigen-specific IgE antibody titer (h-RAST) and peripheral blood eosinophil (Eos) count were measured and compared among atopic subjects and non-atopic controls, and correlations between parameters of atopy and EBV infection were subjected to statistical analysis. Results: Anti-EBV, in particular anti-EBNA antibody titer and AtLy count in peripheral blood were markedly higher in patients with bronchial asthma (BA) and/or atopic dermatitis (AD) than in non-atopic controls, especially in early childhood. No similar findings were obtained for antibodies to cytomegalovirus (CMV). EBV-DNA copy numbers in WBC were elevated in atopic subjects. Correlations between EBV-DNA copy number and other parameters of EBV infection (anti-EBV antibody titer and AtLy count) but those with cytomegalovirus (CMV) infection and markers of atopic disease (IgE, h-RAST level, and Eos count) were demonstrated. It was found that anti-EBNA seronegative atopics have higher copy numbers of EBV DNA in WBC and more elevated levels of IgE and h-RAST than anti-EBNA seropositive atopics. Anti-EBV VCA antibody titer in individuals aged 15 years and younger and anti-EBNA antibody titer among Japanese were suggested to have declined considerably in the past 15 years. Conclusions: The present study suggests that EBV infection in early childhood could precipitate atopic diseases

Late airway obstruction and neutrophil infiltration in sensitized mice after antigen provocation were suppressed by selective and non-selective phosphodiesterase inhibitors

Suppression of antigen-induced late airway obstruction associated with neutrophilic inflammation by selective and non-selective phosphodiesterase (PDE) inhibitors was investigated in mice. Respiratory resistance (Rrs) increased in sensitized BDF1 mice 4-6 h after antigen provocation, whereas no obvious immediate reaction was observed. This reaction was associated with marked airway neutrophilia without significant infiltration of eosinophils. A selective PDE IV inhibitor, T-440 (10-30 mg/kg), and a non-selective PDE inhibitor, theophylline (10 mg/kg), significantly inhibited airway obstruction and neutrophilia when administered orally. An anti-allergic drug, ketotifen (1 mg/kg), caused slight inhibition of airway obstruction, whereas it did not affect airway neutrophilia. These results suggest that neutrophilic inflammation plays a role in the airway obstructive reaction and that PDE has a regulatory role in obstructive airway disease associated with airway inflammation